Establishment and Behavior Evaluation of Rat Chronic Unpredictable Mild Stress and Mouse Social Defeat Models

doi:10.3969/j.issn.2095-1396.2018.01.006

Abstract

Abstract: Objective： To study the pathogenesis of major depressive disorder （MDD），it is necessary to establish animal models of depression. There are two common chronic depressive models that are chronic unpredictable mild stress （CUMS） and social defeat （SD）. In this study，we modified these models and compared the advantages and disadvantages of the two models to establish a more stable model of depression. Methods： For CUMS model，rats were treated with randomized two stressors last for 28 days. Stressors include overnight illumination，tail pinch，wet cage，crowding cage，ice water swimming，water and food deprivation. Rats were divided into three groups of blank Control，CUMS and CUMS + Fluoxetine （10 mg·kg-1） as positive control. For SD model，social defeat stress factors include 5 to 10 min physical attack and 24 hours sensory interaction. Mice were divided into Control and SD groups. After modeling， we adopt sucrose preference，immobility time of Forced Swimming Test and social interaction ratio to study whether the model is successful. Results： There was a significant decrease of sucrose preference （69.3%±3.6%，n=27） and significant increase of immobility time of Forced Swimming Test （131.2±5.8 s，n=27） in CUMS rats，as compared with control group of rats with sucrose preference （81.0%±3.2%，n=17，P<0.05） and immobility time （105.1±8.2 s，n=17， P<0.05）. The sucrose preference （82.1%±3.9%，n=10） and immobility time of Forced Swimming
Test （108.3±9.7 s，n=10） were no significant change in CUMS + Flu group rats，as compared with control group. Mice in social defeat showed that social interaction ratio below 1 （determined by SIR<1，SIR=Duration in interaction zone of target absent phase/ Duration in interaction zone of target present phase），as compared with social interaction ratio greater than 1 in control group. Moreover，SIR of SD mice was significantly lower （69.2%±2.4%，n=16） than that of control group （78.6%±3.2%，n=9，P<0.05）. Conclusions： Based on the core criteria of sucrose preference，models of CUMS in rats and SD in mice are successfully established，whereas the social defeat model is more reproducible and consistent.

Key words: major depressive disorder, chronic unpredictable mild stress model, social defeat, sucrose preference

CLC Number:

R964

XIAO Ting, MA Tian-yang, XU Xiang-qing, WANG Ke-wei. Establishment and Behavior Evaluation of Rat Chronic Unpredictable Mild Stress and Mouse Social Defeat Models[J]. ACTA NEUROPHARMACOLOGICA, 2018, 8(1): 45-53.

References

[1] David V Sheehan, Kazuyuki Nakagome, Yuko Asami, et al. Restoring function in major depressive disorder: A systematic review[J]. J Affect Disord, 2017, 215: 299-313.

[2] Theo Vos, Ryan M Barber, Brad Bell, et al. Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013[J]. Lancet, 2015, 386(9995): 743-800.

[3] The World Health Organization. The world health report 2001[J]. Geneva: WHO 2001: 19-45.

[4] Vikram Patel, Benedict Weobong, Helen A Weiss, et al. The Healthy Activity Program (HAP), a lay counsellor-delivered brief psychological treatment for severe depression, in primary care in India: a randomised controlled trial[J]. Lancet, 2017, 389(10065): 176-185.

[5] David H Overstreet. Modeling depression in animal models[J]. Methods Mol Biol, 2012, 829: 125-144.

[6] Thomas H McCoy, Victor M Castro, Hannah R Rosenfield, et al. A clinical perspective on the relevance of research domain criteria in electronic health records[J]. Am J Psychiatry, 2015, 172(4): 316-320.

[7] John F Cryan, Cedric Mombereau, Annick Vassout. The tail suspension test as a model for assessing antidepressant activity: review of pharmacological and genetic studies in mice[J]. Neurosci Biobehav Rev, 2005, 29(4-5): 571-625.

[8] John F Cryan, C Mombereau. In search of a depressed mouse: utility of models for studying depression-related behavior in genetically modified mice[J]. Mol Psychiatry, 2004, 9(4): 326-357.

[9] Zhou Xin-yu, Liu Lan-xiang, Zhang Yu-qing, et al. Metabolomics identifies perturbations in amino acid metabolism in the prefrontal cortex of the learned helplessness rat model of depression[J]. Neuroscience, 2017, 343: 1-9.

[10] Daniela Velasquez, Caroline Quines, Renan Pistoia, et al. Selective inhibition of MAO-A activity results in an antidepressant-like action of 2-benzoyl 4-iodoselenophene in mice[J]. Physiol Behav, 2017, 170: 100-105.

[11] David Baumeister, Stafford Lightman, Carmine M Pariante. The interface of stress and the HPA axis in behavioural phenotypes of mental illness[J]. Curr Top Behav Neurosci, 2014, 18: 13-24.

[12] Su Chun-lin, Su Chun-wei, Hsiao Ya-Hsin, et al. Epigenetic regulation of BDNF in the learned helplessness-induced animal model of depression[J]. J Psychiatr Res, 2016, 76: 101-110.

[13] Johanna Schoner, Andreas Heinz, Matthias Endres, et al. Post-traumatic stress disorder and beyond: an overview of rodent stress models[J]. J Cell Mol Med, 2017, DOI: 10.1111/jcmm.13161.

[14] Fiona Hollis, Mohamed Kabbaj. Social defeat as an animal model for depression[J]. ILAR J, 2014, 55(2): 221-232.

[15] Qiao Hui, An Shu-cheng, Xu Chang. et al. Role of proBDNF and BDNF in dendritic spine plasticity and depressive-like behaviors induced by an animal model of depression[J]. Brain Res, 2017, 1663: 29-37.

[16] Ryan Wellington Logan, Nicole Edgar, Andrea G Gillman, et al. Chronic stress induces brain region-specific alterations of molecular rhythms that correlate with depression-like behavior in mice[J]. Biol Psychiatry, 2015, 78(4): 249-258

[17] Florent Barthas, Muris Humo, Ralf Gilsbach, et al. Cingulate overexpression of mitogen-activated protein kinase phosphatase-1 as a key factor for depression[J]. Biol Psychiatry, 2017, DOI: 10.1016/j.biopsych.2017.01.019.

[18] Masakazu Ibi, Liu Jun-jie, Noriaki Arakawa, et al. Depressive-like behaviors are regulated by NOX1/NADPH oxidase by redox modification of NMDA receptor 1[J]. J Neurosci, 2017, 37(15): 4200-4212.

[19] Caroline Hammels, Ehsan Pishva, Jochen De Vry, et al. Defeat stress in rodents: From behavior to molecules[J]. Neurosci Biobehav Rev, 2015, DOI: 10.1016/j.neubiorev.2015.10.006.

[20] Sam A Golden, Herbert E Covington, Olivier Berton, et al. A standardized protocol for repeated social defeat stress in mice[J]. Nat Protoc, 2011, 6(8): 1183-1191.

[21] Mailton Vasconcelos, Dirson Joao Stein, Rosa Maria de Almeida. Social defeat protocol and relevant biomarkers, implications for stress response physiology, drug abuse, mood disorders and individual stress vulnerability: a systematic review of the last decade[J]. Trends Psychiatry Psychother, 2015, 37(2): 51-66.

[22] Paul Willner. Reliability of the chronic mild stress model of depression: A user survey[J]. Neurobiol Stress, 2017, 6: 68-77.

[23] Willner P, Towell A, Sampson D, et al. Reduction of sucrose preference by chronic unpredictable mild stress, and its restoration by a tricyclic antidepressant[J]. Psychopharmacology (Berl), 1987, 93(3): 358-364.

[24] Li Wei-dong, Zhu Yan, Shakir M Saud, et al. Electroacupuncture relieves depression-like symptoms in rats exposed to chronic unpredictable mild stress by activating ERK signaling pathway[J]. Neurosci Lett, 2017, 642: 43-50.

[25] Allyson K Friedman, Barbara Juarez, Stacy M Ku, et al. KCNQ channel openers reverse depressive symptoms via an active resilience mechanism[J]. Nat Commun, 2016, 7: 11671.

[26] Shi Hai-shui, Zhu Wei-li, Liu Jian-feng, et al. PI3K/Akt signaling pathway in the basolateral amygdala mediates the rapid antidepressant-like effects of trefoil factor 3[J]. Neuropsychopharmacology, 2012, 37(12): 2671-2683.

[27] Roger D Porsolt, Le Pichon M, Jalfre M. Depression: A new animal model sensitive to anti-depressant treatment[J]. Nature, 1977, 266: 730–732.

[28] Tomoyuki Tashiro, Yuki Murakami, Akihiro Mouri, et al. Kynurenine 3-monooxygenase is implicated in antidepressants-responsive depressive-like behaviors and monoaminergic dysfunctions[J]. Behav Brain Res, 2017, 317: 279-285.

[29] Pirooznia M, Wang T, Avramopoulos D, et al. High-throughput sequencing of the synaptome in major depressive disorder[J]. Mol Psychiatry, 2016, 21(5): 650-655.

[30] Marcus Rothkirch, Jonas Tonn, Stephan Kohler, et al. Neural mechanisms of reinforcement learning in unmedicated patients with major depressive disorder[J]. Brain, 2017, 140(4): 1147-1157.

[31] Matthew J Robson, Meagan A Quinlan, Randy D Blakely. Immune system activation and depression: roles of serotonin in the central nervous system and periphery[J]. ACS Chem Neurosci, 2017, 8(5): 932-942.